ArticleHuman molecular genetics2018
The pro-apoptotic JNK scaffold POSH/SH3RF1 mediates CHMP2BIntron5-associated toxicity in animal models of frontotemporal dementia.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Association between cerebral lesions and the severity of diabetic cardiovascular disease, retinopathy, and nephropathy-new lessons to learn from neuroimaging.Journal of endocrinological investigation · 2025Review
- The role of SH3RF2 in lung squamous cell carcinoma and M2 polarization: insights into LZTS2 ubiquitination.Biology direct · 2025Article
- Tau fibrils induce nanoscale membrane damage and nucleate cytosolic tau at lysosomes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- Neuroprotective activity of ursodeoxycholic acid in CHMP2BNeurobiology of disease · 2020Article
- JNK signalling regulates antioxidant responses in neurons.Redox biology · 2020Article
- Retrovirus reactivation in CHMP2BIntron5 models of frontotemporal dementia.Human molecular genetics · 2020Article
- Co-expression of C9orf72 related dipeptide-repeats over 1000 repeat units reveals age- and combination-specific phenotypic profiles in Drosophila.Acta neuropathologica communications · 2020Article
- Ik2/TBK1 and Hook/Dynein, an adaptor complex for early endosome transport, are genetic modifiers of FTD-associated mutant CHMP2B toxicity in Drosophila.Scientific reports · 2020Article
- Molecular Genetics of Frontotemporal Dementia Elucidated byInternational journal of molecular sciences · 2018Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Frontotemporal dementia (FTD) is one of the most prevalent forms of early-onset dementia. However, the pathological mechanisms driving neuronal atrophy in FTD remain poorly understood. Here we identify a conserved role for the novel pro-apoptotic protein plenty of SH3s (POSH)/SH3 domain containing ring finger 1 in mediating neuropathology in Drosophila and mammalian models of charged multivesicular body protein 2B (CHMP2BIntron5) associated FTD. Aberrant, AKT dependent, accumulation of POSH was observed throughout the nervous system of both Drosophila and mice expressing CHMP2BIntron5. Knockdown of POSH was shown to be neuroprotective and sufficient to alleviate aberrant neuronal morphology, behavioral deficits and premature-lethality in Drosophila models, as well as dendritic collapse and cell death in CHMP2BIntron5expressing rat primary neurons. POSH knockdown also ameliorated elevated markers of Jun N-terminal kinase and apoptotic cascades in both Drosophila and mammalian models. This study provides the first characterization of POSH as a potential component of an FTD neuropathology, identifying a novel apoptotic pathway with relevance to the FTD spectrum.
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